A reduced autonomic balance during heart failure has been shown to be associated with left ventricular dysfunction and increased mortality. This reduced autonomic balance increases sympathetic and decreases parasympathetic cardiac tone. Direct stimulation of the vagal parasympathetic fibers has been shown to reduce heart rate via activation of the parasympathetic nervous system and indirect inhibition of the sympathetic nervous system. Some data indicate that increasing parasympathetic tone and reducing sympathetic tone may protect the myocardium from further remodeling and predisposition to fatal arrhythmias following myocardial infarction; and some data indicates that chronic stimulation of the vagus nerve may protect the myocardium following cardiac ischemic insult. However, implantation of electrodes is an invasive procedure, and it can be difficult to immediately implant electrodes after a myocardial infarction.
The auricular nerve is a branch of the vagus nerve that passes near the external auditory canal immediately behind the ear. Stimulation of this nerve branch depolarizes the vagus and elicits bradycardia. Needle puncture electrodes have been used to stimulate the auricular branch of the vagus nerve. The needle puncture electrodes punctured the skin to a depth of 0.1-0.3 mm in the area situated near the auditory passage that contains endings of the nerve auricularis. The neural stimulation applied by these needle puncture electrodes to the auricular branch improved anginal symptoms, improved coronary blood flow, increased ejection fraction and reduced the incidence of developing congestive heart failure (CHF).